Abstract
The photoreceptor UV RESISTANCE LOCUS 8 (UVR8) specifically mediates photomorphogenic responses to UV-B wavelengths. UVR8 acts by regulating transcription of a set of genes, but the underlying mechanisms are unknown. Previous research indicated that UVR8 can associate with chromatin, but the specificity and functional significance of this interaction are not clear. Here we show, by chromatin immunoprecipitation, that UV-B exposure of Arabidopsis increases acetylation of lysines K9 and/or K14 of histone H3 at UVR8-regulated gene loci in a UVR8-dependent manner. The transcription factors HY5 and/or HYH, which mediate UVR8-regulated transcription, are also required for this chromatin modification, at least for the ELIP1 gene. Furthermore, sequencing of the immunoprecipitated DNA revealed that all UV-B-induced enrichments in H3K9,14diacetylation across the genome are UVR8-dependent, and approximately 40 % of the enriched loci contain known UVR8-regulated genes. In addition, inhibition of histone acetylation by anacardic acid reduces the UV-B induced, UVR8 mediated expression of ELIP1 and CHS. No evidence was obtained in yeast 2-hybrid assays for a direct interaction between either UVR8 or HY5 and several proteins involved in light-regulated histone modification, nor for the involvement of these proteins in UVR8-mediated responses in plants, although functional redundancy between proteins could influence the results. In summary, this study shows that UVR8 regulates a specific chromatin modification associated with transcriptional regulation of a set of UVR8-target genes.Electronic supplementary materialThe online version of this article (doi:10.1007/s11103-016-0522-3) contains supplementary material, which is available to authorized users.
Highlights
Plants are immobile autotrophs whose optimal growth and development relies heavily on light
Chromatin was immunoprecipitated with an antibody recognising H3K9,14diac and control ChIP experiments were performed with an antibody against an invariant histone H3 domain (Supplementary Fig. S1) to demonstrate that the Ultraviolet-B light (UV-B) treatment did not cause chromatin immunoprecipitation (ChI P)-detectable changes in nucleosome occupancy, which if present would pose a problem for the interpretation of the data
ACT2 was used as a reference gene for normalisation of the amount of the ChIPed material and WRKY30, a gene induced through stress-related UV RESI STANCE LOCUS 8 (UVR8)-independent UV-B responses, was chosen as a control to assess whether the threshold separating the photomorphogenic from the stressful stimulus was exceeded during the UV-B treatments
Summary
Plants are immobile autotrophs whose optimal growth and development relies heavily on light. Ultraviolet-B light (UV-B; 280–315 nm) is a minor component of the solar spectrum, but regulates several aspects of plant development (Jenkins 2009; Jansen and Bornman 2012). The only known UV-B photoreceptor is UV RESI STANCE LOCUS 8 (UVR8), which employs a unique photosensory mechanism for light absorption and initiation of the signalling events that lead eventually to particular physiological responses (Jenkins 2014a, b; Ulm and Jenkins 2015). Structural characterization of UVR8 (Christie et al 2012; Wu et al 2012) revealed that it does not employ an external chromophore, but instead uses intrinsic tryptophan amino acids for UV-B photoreception (Rizzini et al 2011; O’Hara and Jenkins 2012; Mathes et al 2015; Wu et al 2015).
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